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Long-lasting antiallodynic effects of IMT504 in rats with spared nerve injury relate to strengthened migration of mesenchymal stem cells towards injured nerves

Mailín Casadei

  • Derqui,
  • Argentina
  • Mailín Casadei ¹
  • , Esteban Juan Fiore ²
  • , Candelaria Leiguarda ¹
  • , Julia Rubione ¹
  • , Florencia Coronel ³
  • , Mariana García ²
  • , Guillermo Mazzolini ²
  • , Marcelo Villar ¹
  • , Alejandro Montaner ⁴
  • , Pablo Brumovsky ¹
  • 1 Acute and Chronic Pain Laboratory, Instituto de Investigaciones en Medicina Traslacional (IIMT), Universidad Austral-CONICET, Av. Juan D. Perón 1500, Derqui, Pilar, Buenos Aires, Argentina.
  • 2 Gene Therapy Laboratory, Instituto de Investigaciones en Medicina Traslacional (IIMT), Universidad Austral-CONICET, Av. Juan D. Perón 1500, Derqui, Pilar, Buenos Aires, Argentina.
  • 3 Pain in Cancer Laboratory, Instituto de Investigaciones en Medicina Traslacional (IIMT), Universidad Austral-CONICET, Av. Juan D. Perón 1500, Derqui, Pilar, Buenos Aires, Argentina.
  • 4 Instituto de Ciencia y Tecnología "Dr. César Milstein", CONICET, Fundación Pablo Cassará, Ciudad Autónoma de Buenos Aires, Argentina.

Peripheral neuropathic pain is caused by injury or dysfunction of peripheral nerves, and is characterized by allodynia and hyperalgesia. Neuropathic pain is complex and difficult to treat, in many cases resistant to currently available pain drugs. We have shown that multiple systemic doses of the oligodeoxynucleotide (ODN) IMT504 result in clear and long-lasting antiallodynic and anti-inflammatory effects in rats with unilateral sciatic nerve crush or hindpaw inflammation. Interestingly, in rats with sciatic nerve crush, virtually identical allodynia-preventing effects were observed after systemic administration of IMT504 or exogenous rat bone marrow mesenchymal stem cells (BMMSC). Here, we address the role of IMT504 in a model of chronic neuropathic pain, and the involvement of BMMSC.
Early or late IMT504 administration revert mechanical and cold allodynia in animals undergoing persistent neuropathic pain. The effect exhibits a considerably quick onset and is long-lasting. The ODN also appears to potentiate the mobilization, migration and homing of BMMSCs into injured nerves. If these effects on BMMSCs relate to the antiallodynic actions of IMT504, it remains to be further demonstrated. However, our results support the idea that this ODN could be a promising therapeutic agent in the treatment of chronic neuropathic pain, also in humans.

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